Daniel Fischer
CEO
Tevard
Tevard Biosciences develops suppressor tRNA therapeutics delivered via AAV vectors to enable ribosomal read‑through of premature stop codons, restoring full‑length protein production in cells that naturally express the defective gene. The gene‑agnostic platform can target any gene with nonsense mutations, allowing a single therapy to address multiple rare diseases and supporting basket clinical trials. Preclinical models have shown durable protein rescue for conditions such as dilated cardiomyopathy and Duchenne muscular dystrophy.
- Biotechnology
Updated 5 months ago
Funding
Raised to date
$47.9MRaised to date based on public sources. This may differ from the amount the company actually raised and is based only on what is publicly available on the internet.
Funding rounds are not available yet.
Founders
Product
Problem
Many rare genetic diseases are caused by nonsense mutations that introduce premature stop codons, preventing cells from producing full-length functional proteins. Existing therapies often target individual genes, are limited to specific mutations, or produce truncated proteins, leaving most patients without disease‑modifying options.
Solution
Tevard Biosciences develops suppressor tRNA therapeutics delivered via adeno‑associated virus (AAV) to enable ribosomal read‑through of premature stop codons. By supplying engineered tRNAs that recognize nonsense codons, the platform restores translation of full‑length proteins in the cells that naturally express the defective gene. This approach is gene‑size agnostic and can address multiple diseases that share the same class of mutation, allowing for basket clinical trials and broader label expansions. Preclinical studies have demonstrated full‑length protein rescue for titin in cardiomyopathy, dystrophin in Duchenne muscular dystrophy, and other targets across organ systems, offering a durable, endogenous‑level correction without risk of overexpression.
Target Audience
Primary customers are pharmaceutical and biotech companies developing treatments for rare inherited diseases caused by nonsense mutations, as well as academic and clinical research programs seeking a platform for durable protein restoration.
Features
- Engineered suppressor tRNAs that specifically decode premature stop codons, enabling full‑length protein synthesis.
- AAV vector delivery provides long‑lasting expression of the therapeutic tRNA in target tissues.
- Gene‑agnostic modality: a single suppressor tRNA can treat any gene harboring the same nonsense mutation class.
- Protein restoration limited to cells naturally expressing the defective gene, preserving physiological regulation.
- No risk of protein overexpression because the therapy relies on endogenous translation mechanisms.
- Demonstrated efficacy in mouse models of dilated cardiomyopathy (TTN) and Duchenne muscular dystrophy (dystrophin).